NIDCR 2015 Seymour J. Kreshover Lecture
Dr. Linda Watkins is a University of Colorado President's Teaching Scholar and the Director of the Interdepartmental Neuroscience PhD Program. She has held several NIH research grants, including grants from NIDCR, NIDA, NIMH, and NINDS.
Dr. Watkins’ research is focused on how to control chronic pain and increase the effectiveness of analgesics while minimizing their side effects. When non-neuronal cells known as glia are activated, they can create persistent, amplified neuroinflammation, thereby promoting the transition from acute to chronic pain. Dr. Watkins’ work has shown that glial activation can also compromise the ability of opioids to suppress chronic pain, contributing to the development of drug tolerance and dependence. Her findings have advanced our understanding of how therapeutics that target a specific glial activation receptor are effective stand-alone treatments for chronic pain and can also increase the efficacy of opioids while decreasing analgesic tolerance and dependence. Two such drugs, developed in the Watkins lab, are moving toward clinical trials.
NIDCR established the NIDCR Seymour J. Kreshover Lecture as a tribute to the late Seymour Kreshover, DDS, MD, PhD, who served as director of the (then) National Institute of Dental Research from 1966–1975. Lectures are delivered by outstanding investigators who have made significant contributions to research that impacts the dental, oral, and craniofacial field.
For more information go to http://www.nidcr.nih.gov/NewsAndFeatures/Announcements/Kreshover-2015.htm
Air date: 5/4/2015 2:00:00 PM
Neuroscience Seminar Series
Air date: 6/1/2015 12:00:00 PM
Neuroscience Seminar Series
Air date: 6/15/2015 12:00:00 PM
Neuroscience Seminar Series
Air date: 6/8/2015 12:00:00 PM
Immunology Interest Group
Dr. Steve Rosenberg received his B.A. and M.D. degrees at Johns Hopkins University and a Ph.D. in Biophysics at Harvard University. After completing his residency training in surgery in 1974 at the Peter Bent Brigham Hospital in Boston, Massachusetts, Dr. Rosenberg became the Chief of Surgery at the NCI, NIH, a position he has held to the present time. Dr. Rosenberg has pioneered the development of effective immunotherapies and gene therapies for patients with advanced cancers. His studies of the adoptive transfer of genetically modified lymphocytes have resulted in the regression of metastatic cancer in patients with melanoma, sarcomas and lymphomas. His current research is aimed at defining the host immune response of patients to their cancers. These studies emphasize the ability of human lymphocytes to recognize unique cancer antigens and the identification of anti-tumor T cell receptors that can be exploited to develop new cell transfer immunotherapies for the treatment of cancer patients. Dr. Rosenberg also oversees the Surgery Branch’s clinical program aimed at translating scientific advances into effective immunotherapies for patients with cancer.
For more information go to http://sigs.nih.gov/immunology/Pages/default.aspx
Air date: 4/29/2015 4:15:00 PM
NCI Center for Cancer Research Grand Rounds
Dr. Chi Van Dang is Director of the Abramson Cancer Center of the University of Pennsylvania, Professor of Medicine, and the John H. Glick Professor. As Director of the Abramson Cancer Center, he launched a series of Translational Centers of Excellence, which propels teams of scientists, nurses, and clinicians to reach for the cure for various cancers. He also catalyzed the establishment of the Center for Personalized Diagnostics with Penn’s Department of Pathology and the Basser Research Center for BRCA. His career at Penn started in September 2011 after having been at Johns Hopkins, where he was the Johns Hopkins Family Professor in Oncology Research and Vice Dean for Research of Johns Hopkins University School of Medicine. He directed the Hopkins Institute for Cell Engineering and was a Professor of Medicine, Pathology, Oncology, and Cell Biology with joint appointment in Molecular Biology and Genetics. Dr. Dang is Editor-in-Chief of Cancer & Metabolism and serves or served on editorial boards of Cancer Discovery, Cancer Research, Clinical Translational Science, Current Cancer Therapy Reviews, eLIFE, Journal of Clinical Investigation, Journal of Molecular Medicine, Genes & Cancer, Molecular and Cellular Biology, Neoplasia, and Oncotargets. He has authored over 200 scientific and medical articles, book chapters and a book. He is a member of the Institute of Medicine of the National Academy of Sciences, American Academy of Arts & Sciences, National Cancer Institute Board of Scientific Advisors, American Society for Clinical Investigation (ASCI) and The Association of American Physicians. He was president of the ASCI (2003). He held an NIH/National Cancer Institute MERIT award, received a number of honors, and sponsored and mentored many NIH K08 physician-scientist awardees, Ph.D. doctorates and post-doctoral fellows. The Dang laboratory has contributed to the understanding of the function of the MYC cancer gene, which has emerged as a central transcription factor or gene switch in many different human cancers. His laboratory established the first mechanistic link between the MYC cancer gene and cellular energy metabolism, contributing to the concept that genetic alterations in cancers re-program fuel utilization by tumors and render cancers addicted to certain fuel sources. His laboratory is now exploiting these concepts for therapeutic targeting of cancer cell metabolism as a new way to treat cancer.
For more information go to https://ccrod.cancer.gov/ccrlectures
Air date: 5/1/2015 12:00:00 PM
Wednesday Afternoon Lecture Series
Successful fetal and maternal outcomes in the context of maternal pregestational diabetes (type 1 or type 2) largely depend on how well glycemic control is maintained, especially prior to conception and in the first trimester of pregnancy. Stringent metabolic control and monitoring, and nutritional management via supplements and antioxidants significantly reduce the risk for or can eliminate poor outcomes due to hyperglycemia on both the maternal and fetal side.
Experiments in animal models have shown that hyperglycemia induces oxidative stress within the developing cells and tissues of the fetus. As maternal glucose concentration increases, so does the concentration of reactive oxygen species (ROS) within the fetus. When ROS concentration increases, the natural antioxidant capacity of fetal cells decreases, which leads to at least three biomolecular events causing birth defects: membrane alterations; mitochondrial dysfunction; and initiation of apoptosis.
Studies using mice that are genetically modified to overexpress the human antioxidant superoxide dismutase have shown that combating oxidative stress in a diabetic pregnant mouse model is possible, and that antioxidants can reduce the rate of hyperglycemia-induced malformations. In addition, blocking cell-death pathways, by inhibiting pro-apoptotic signaling proteins, can prevent birth defects. More recent work has explored the use of naturally-occurring proteins and compounds to reduce maternal diabetes-induced oxidative stress.
Although epidemiological studies examining the benefits of these interventions are needed, the push to translate basic-science findings into preclinical and rigorous clinical studies has made more effective interventions and prevention strategies for diabetes and its complications very close to becoming clinical practice realities.
For more information go to http://wals.od.nih.gov
Air date: 4/29/2015 3:00:00 PM
PMI Working Group
For more information go to http://acd.od.nih.gov
Air date: 4/29/2015 8:30:00 AM